Evidence map›Paper›PMID 24500875›Full record

ArticleDevelopmental dynamics : an official publication of the American Association of Anatomists2014

Tropomyosin is required for cardiac morphogenesis, myofibril assembly, and formation of adherens junctions in the developing mouse embryo.

Caroline R McKeown, Roberta B Nowak, David S Gokhin, Velia M Fowler

Abstract read
In one paragraph

Article in Developmental dynamics : an official publication of the American Association of Anatomists, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.6field-weighted citation impact, top 16% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Structural and Functional Properties of Kappa Tropomyosin.International journal of molecular sciences · 2023
    Article
  5. Article
  6. Article
  7. Article
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  9. Mutations in RNA Methyltransferase GeneFrontiers in cell and developmental biology · 2021
    Article
  10. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Caroline R McKeownDepartment of Cell and Molecular Biology, The Scripps Research Institute, La Jolla, California.
Roberta B Nowak
David S Gokhin
Velia M Fowler
Scripps Research Institute · US

Funding

Capping Actin Growth in Erythroid and Nonerythroid CellsR01HL083464 · NHLBI · UNIVERSITY OF DELAWARE · PI FOWLER, VELIA M · 2006 to 2019
$7.1M
Core--ProteomicsP30EY012598 · NEI · SCRIPPS RESEARCH INSTITUTE · PI FRIEDLANDER, MARTIN · 2001 to 2005
$3.6M
San Diego Skeletal Muscle Research CenterP30AR061303 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CHEN, JU · 2011 to 2015
$3.3M
VASCULAR BIOLOGY, THROMBOSIS, AND HEMOSTASIST32HL007695 · NHLBI · SCRIPPS RESEARCH INSTITUTE · PI QUIGLEY, JAMES P · 1991 to 2005
$1.9M
NEI NIH HHS P30 EY012598NEI NIH HHS P30-EY12598NHLBI NIH HHS R01 HL083464NHLBI NIH HHS R01-HL083464NHLBI NIH HHS T32 HL007695NHLBI NIH HHS T32-HL07695NIAMS NIH HHS P30 AR061303NIAMS NIH HHS P30-AR061303
6 · The paper itself

Abstract

backgroundWe explored a function for tropomyosin (TM) in mammalian myofibril assembly and cardiac development by analyzing a deletion in the mouse TPM1 gene targeting αTM1, the major striated muscle TM isoform.

resultsMice lacking αTM1 are embryonic lethal at E9.5 with enlarged, misshapen, and non-beating hearts characterized by an abnormally thin myocardium and reduced trabeculae. αTM1-deficient cardiomyocytes do not assemble striated myofibrils, instead displaying aberrant non-striated F-actin fibrils with α-actinin puncta dispersed irregularly along their lengths. αTM1's binding partner, tropomodulin1 (Tmod1), is also disorganized, and both myomesin-containing thick filaments as well as titin Z1Z2 fail to assemble in a striated pattern. Adherens junctions are reduced in size in αTM1-deficient cardiomyocytes, α-actinin/F-actin adherens belts fail to assemble at apical cell-cell contacts, and cell contours are highly irregular, resulting in abnormal cell shapes and a highly folded cardiac surface. In addition, Tmod1-deficient cardiomyocytes exhibit failure of α-actinin/F-actin adherens belt assembly.

conclusionsAbsence of αTM1 resulting in unstable F-actin may preclude sarcomere formation and/or lead to degeneration of partially assembled sarcomeres due to unregulated actomyosin interactions. Our data also identify a novel αTM1/Tmod1-based pathway stabilizing F-actin at cell-cell junctions, which may be required for maintenance of cell shapes during embryonic cardiac morphogenesis.

Indexed as

Adherens JunctionsAnimalsCell CommunicationEmbryo, MammalianHeartMiceMice, KnockoutMorphogenesisTropomyosinTpm1 protein, mouseTropomyosincardiomyocytecell junctionheartmyofibrillogenesismyomesinthin filamenttitintropomodulin1α-actinin

Identifiers

PMID24500875
PMCPMC4031292
OpenAlexW1596180176

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.